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Type I interferons (IFNs) function as the first line of defense against viral infections by modulating numerous biological processes to establish an antiviral state and influencing the activation of various immune cells. During influenza A infection, the NS1 encoded by the virus genome disrupts many cellular processes to block type I IFN responses. We show that expression of H5N1 NS1 in HeLa cells reduces IFN-inducible activation of STAT proteins and its subsequent binding to DNA complexes. Subsequent analysis suggests NS1 blocks IFN signaling by inhibiting expression of type I IFN receptor subunit, IFNAR1, as well as up-regulating SOCS1 expression. Finally, we demonstrate that pretreatment of primary human lung tissue with IFN alfacon-1 inhibits H5N1 viral replication by up-regulating a number of interferon-stimulated genes. The data suggest that NS1 can directly interfere with Type I IFN signaling, and that pretreatment with IFN can inhibit H5N1 infection in primary human lung tissue.

Type I interferons (IFNs) function as the first line of defense against viral infections by modulating numerous biological processes to establish an antiviral state and influencing the activation of various immune cells. During influenza A infection, the NS1 encoded by the virus genome disrupts many cellular processes to block type I IFN responses. We show that expression of H5N1 NS1 in HeLa cells reduces IFN-inducible activation of STAT proteins and its subsequent binding to DNA complexes. Subsequent analysis suggests NS1 blocks IFN signaling by inhibiting expression of type I IFN receptor subunit, IFNAR1, as well as up-regulating SOCS1 expression. Finally, we demonstrate that pretreatment of primary human lung tissue with IFN alfacon-1 inhibits H5N1 viral replication by up-regulating a number of interferon-stimulated genes. The data suggest that NS1 can directly interfere with Type I IFN signaling, and that pretreatment with IFN can inhibit H5N1 infection in primary human lung tissue.

Diss. (sammanfattning) Umeå : Univ., 2004. / Härtill 3 uppsatser.

Frankfurt (Main), Universiẗat, Diss., 2007.

Univ., Diss.--Hannover, 1999.

Thesis (Ph. D., Microbiology, Molecular Biology and Biochemistry)--University of Idaho, August 2008. / Major professor: Kurt E. Gustin. Includes bibliographical references. Also available online (PDF file) by subscription or by purchasing the individual file.

Thesis (M.S.) in Microbiology--University of Maine, 2003. / Includes vita. Includes bibliographical references (leaves 69-78).

Thesis (M. Phil.)--University of Hong Kong, 2000. / Cover title. Includes bibliographical references (leaves 118-135).

Thesis (M. Phil.)--University of Hong Kong, 2002. / Includes bibliographical references (leaves 122-139).